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:: Volume 30, Issue 2 (Bimothly 2026) ::
Feyz Med Sci J 2026, 30(2): 3-3 Back to browse issues page
Protective Effects of L-Glutathione Against Imidacloprid-Induced Oxidative Damage and Neurochemical Alterations in Rat Brain
Mohammad Sina Mirjani , Mohammad Reza Khaksar *
Research Center for Environmental Pollutants, Qom University of Medical Sciences, Qom, Iran , mrkhaksar@muq.ac.ir
Abstract:   (410 Views)
Background and Aim: Exposure to imidacloprid induces neural damage through enhanced production of reactive oxygen species, increased lipid peroxidation, and disruption of antioxidant defense systems. L-Glutathione, an endogenous antioxidant, plays a crucial role in maintaining redox balance and protecting neuronal cells. This study aimed to investigate the protective effect of L-glutathione against oxidative stress and neural damage induced by subacute imidacloprid exposure in rat brain.
Methods: In this experimental study, 24 adult male Wistar rats were divided into four groups (n = 6 each): control, imidacloprid-treated group (45 mg/kg; one-tenth LD50), L-glutathione-treated group (100 mg/kg), and combined imidacloprid + L-glutathione group. All treatments were administered daily via gavage for 28 days. At the end of the experiment, brain tissues were collected, and oxidative stress biomarkers including malondialdehyde (MDA), reduced glutathione (GSH), total antioxidant capacity (TAC), antioxidant enzyme activities (GPx, GSR, GST, SOD, and CAT), and acetylcholinesterase (AChE) activity were measured.
Results: Imidacloprid administration significantly decreased AChE activity, TAC, GSH levels, and the activities of GPx, GSR, and GST, while significantly increasing MDA levels and SOD activity (p < 0.05). Catalase activity showed no significant change. L-glutathione alone moderately increased TAC and the activity of certain antioxidant enzymes. In the combined group, L-glutathione markedly improved oxidative and neurochemical parameters, with significant reductions in lipid peroxidation and enhancement of antioxidant defenses (P < 0.05).
Conclusion: The findings demonstrate that subacute exposure to imidacloprid induces oxidative stress and neurofunctional impairment in rat brain. L-glutathione administration mitigates these neurotoxic effects by enhancing antioxidant defense systems, reducing oxidative damage, and modulating AChE activity. These results support the potential neuroprotective role of L-glutathione against imidacloprid-induced toxicity.
Keywords: Imidacloprid, L-glutathione, Oxidative stress, Neurotoxicity, Brain
     
Type of Study: Research | Subject: General
Received: 2026/02/16 | Revised: 2026/07/1 | Accepted: 2026/05/17 | Published: 2026/07/1
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Mirjani M S, Khaksar M R. Protective Effects of L-Glutathione Against Imidacloprid-Induced Oxidative Damage and Neurochemical Alterations in Rat Brain. Feyz Med Sci J 2026; 30 (2) :3-3
URL: http://feyz.kaums.ac.ir/article-1-5503-en.html


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Volume 30, Issue 2 (Bimothly 2026) Back to browse issues page
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